IL-17–producing ST2+ group 2 innate lymphoid cells play a pathogenic role in lung inflammation

Cai, Ting; Qiu, Jinxin; Ji, Yan; Li, Wenjing; Ding, Zhaoyun; Suo, Caixia; Chang, Jiali; Wang, Jingjing; He, Rui; Qian, Youcun; Guo, Xiaohuan; Zhou, Liang; Sheng, Huiming; Shen, Lei; Qiu, Ju

doi:10.1016/j.jaci.2018.03.007

Cited by 103 publications

(107 citation statements)

References 60 publications

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“…In addition, LTC4 and LTD4 have a synergistic effect on ILC2s in combination with IL‐33. It has also been recently shown that a combination of IL‐33 with LTC4 or LTD4 can induce IL‐17 expression in ILC2s . Mechanistically, the activation of CysLT1R rapidly increases intracellular Ca 2+ in ILC2s and promotes the nuclear translocation of NFAT.…”

Section: Lipid Mediators (Ltc4 Ltd4 Lte4 Ltb4 Lxa4 Pgd2 Pge2 Amentioning

confidence: 98%

The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

Kabata

Moro

Koyasu

2018

Immunological Reviews

229

183

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Summary Group 2 innate lymphoid cells (ILC2s) play critical roles in the induction of type 2 inflammation, response to parasite infection, metabolic homeostasis, and tissue repair. These multifunctional roles of ILC2s are tightly controlled by complex regulatory systems in the local microenvironment, the disruption of which may cause various health problems. This review summarizes up‐to‐date knowledge regarding positive and negative regulators for ILC2s based on their function and signaling pathways, including activating cytokines (IL‐33, IL‐25; MAPK, NF‐κB pathways), co‐stimulatory cytokines (IL‐2, IL‐7, IL‐9, TSLP; STAT5, IL‐4; STAT6, TNF superfamily; MAPK, NF‐κB pathways), suppressive cytokines (type1 IFNs, IFN‐γ, IL‐27; STAT1, IL‐10, TGF‐β), transdifferentiation cytokines (IL‐12; STAT4, IL‐1β, IL‐18), lipid mediators (LTC4, LTD4, LTE4, PGD2; Ca2+‐NFAT pathways, PGE2, PGI2; AC/cAMP/PKA pathways, LXA4, LTB4), neuropeptides (NMU; Ca2+‐NFAT, MAPK pathways, VIP, CGRP, catecholamine, acetylcholine), sex hormones (androgen, estrogen), nutrients (butyrate; HDAC inhibitors, vitamins), and cell‐to‐cell interactions (ICOSL‐ICOS; STAT5, B7‐H6‐NKp30, E‐cadherin‐KLRG1). This comprehensive review affords a better understanding of the regulatory network system for ILC2s, providing impetus to develop new treatment strategies for ILC2‐related health problems.

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Section: Lipid Mediators (Ltc4 Ltd4 Lte4 Ltb4 Lxa4 Pgd2 Pge2 Amentioning

confidence: 98%

The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

Kabata

Moro

Koyasu

2018

Immunological Reviews

229

183

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“…After BAL, lungs were dissected into pieces for enzyme digestion in RPMI-1640 medium containing DNase I (0.15 mg/mL, Sigma, USA) and collagenase II (1 mg/mL, Sigma, USA) at 37 ℃ for 1 h [27,28]. The digested tissues were homogenized by vigorous shaking and passed through a 70-μm cell strainer (BD, USA).…”

Section: Preparation Of Lung Single Cell Suspensionsmentioning

confidence: 99%

Manipulation of macrophage polarization by peptide-coated gold nanoparticles and its protective effects on acute lung injury

et al. 2020

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Background: Macrophage polarization and reprogramming in the lung play a critical role in the initiation, development and progression of acute lung injury (ALI). Regulating the activation and differentiation of pulmonary macrophages may provide a potential therapeutic strategy to treat ALI. We previously developed a novel class of antiinflammatory nanoparticles (P12) that can potently inhibit Toll-like receptor (TLR) signaling in macrophages. These bioactive nanodevices were made of gold nanoparticles (GNPs) coated with hexapeptides to not only ensure their physiological stability but also enable GNPs with TLR inhibitory activity.Results: In this study, using a lipopolysaccharide (LPS) induced ALI mouse model, we showed that P12 was able to alleviate lung inflammation and damage through reducing the infiltration of inflammatory cells and increasing the anti-inflammatory cytokine (IL-10) in the lung. These results prompted us to investigate possible macrophage polarization by P12. We first confirmed that P12 primarily targeted macrophages in the lung to exert anti-inflammatory activity. We then showed that P12 could drive the polarization of mouse bone marrow-derived macrophages (BMDMs) toward anti-inflammatory M2 phenotype. Interestingly, in the ALI mouse model, P12 was able to increase the alveolar M2 macrophages and reduce both the alveolar and interstitial M1 macrophages in the bronchoalveolar lavage fluid (BALF) and lung tissues. Conclusion:This study demonstrated that peptide-coated GNPs could induce M2 macrophage polarization in vitro and in vivo to effectively regulate lung inflammation, protect lung from injuries and promote inflammation resolution. The ability of regulating macrophage polarization together with TLR inhibition made such a bioactive nanodevice a new generation of potent therapeutics to treat ALI.

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“…110 Interestingly, IL-17-producing ILC2s play a pathogenic role in a mouse model of lung allergy. 111 At the molecular level, the transcription factors Bcl11b and Gfi-1 regulate the identity of ILC2s by repressing the expression of RORγt and its associated genes. Therefore, deletion of Bcl11b or Gfi-1 in ILC2s results in IL-17 production and loss of GATA3, IL-5, and IL-13 expression.…”

Section: Type 2 Immune Response Mediated By Ilc2smentioning

confidence: 99%

Orchestration between ILC2s and Th2 cells in shaping type 2 immune responses

2019

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The type 2 immune response is critical for host defense against large parasites such as helminths. On the other hand, dysregulation of the type 2 immune response may cause immunopathological conditions, including asthma, atopic dermatitis, rhinitis, and anaphylaxis. Thus, a balanced type 2 immune response must be achieved to mount effective protection against invading pathogens while avoiding immunopathology. The classical model of type 2 immunity mainly involves the differentiation of type 2 T helper (Th2) cells and the production of distinct type 2 cytokines, including interleukin-4 (IL-4), IL-5, and IL-13. Group 2 innate lymphoid cells (ILC2s) were recently recognized as another important source of type 2 cytokines. Although eosinophils, mast cells, and basophils can also express type 2 cytokines and participate in type 2 immune responses to various degrees, the production of type 2 cytokines by the lymphoid lineages, Th2 cells, and ILC2s in particular is the central event during the type 2 immune response. In this review, we discuss recent advances in our understanding of how ILC2s and Th2 cells orchestrate type 2 immune responses through direct and indirect interactions. Keywords: Type 2 immune response; type 2 T helper cell (Th2); Group 2 innate lymphoid cell (ILC2); Allergy and asthma Cellular & Molecular Immunology (2019) 16:225-235; https://doi.

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IL-17–producing ST2+ group 2 innate lymphoid cells play a pathogenic role in lung inflammation

Abstract: During lung inflammation, IL-33 and leukotrienes synergistically induce ILC2s. ILC2s are a highly pathogenic and unexpected source for IL-17 in lung inflammation.

Cited by 103 publications

References 60 publications

The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

Manipulation of macrophage polarization by peptide-coated gold nanoparticles and its protective effects on acute lung injury

Orchestration between ILC2s and Th2 cells in shaping type 2 immune responses

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